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Background: Coronary slow flow (CSF) is an angiographic entity characterized by delayed coronary opacification with no evident obstructive lesion in the epicardial coronary artery. Several studies have shown that the occurrence and development of CSF may be closely related to inflammation. Soluble vascular cell adhesion molecule-1 (sVCAM-1) is a biomarker related to inflammation. The aim of this study was to evaluate the correlation between plasma soluble VCAM-1 level and CSF occurrence and thus the predictive value of VCAM-1 for CSF. Methods: Forty-six CSF patients and thirty control subjects were enrolled. Corrected thrombolysis in myocardial infarction frame count (cTFC) was used to diagnose CSF. Functional status and quality of life were determined by the Seattle Angina Questionnaire (SAQ). Echocardiography was used to evaluate the systolic and diastolic function of the left ventricle (LV) and right ventricle (RV). The plasma levels of sVCAM-1, IL-6, and TNF-α were quantified by enzyme-linked immunosorbent assay. Results: Compared with the control group, the physical limitation score by the SAQ, the LV global longitudinal strain (GLS), mitral E, and mitral E/A decreased in patients with CSF, while the plasma IL-6 and TNF-α levels increased. The plasma sVCAM-1 level in the CSF group was significantly higher than that in the control group (186.03 ± 83.21 vs. 82.43 ± 42.12 ng/mL, p < 0.001), positively correlated with mean cTFC (r = 0.57, p < 0.001), and negatively correlated with the physical limitation score (r = −0.32, p = 0.004). Logistic regression analyses confirmed that plasma sVCAM-1 level (OR = 1.07, 95%CI: 1.03–1.11) is an independent predictor of CSF, and the receiver operating characteristic curve analysis showed that plasma sVCAM-1 levels had statistical significance in predicting CSF (area under curve = 0.88, p < 0.001). When the sVCAM-1 level was higher than 111.57 ng/mL, the sensitivity for predicting CSF was 87% and the specificity was 73%. Conclusions: Plasma sVCAM-1 level can be used to predict CSF and was associated with the clinical symptoms of patients. It may serve as a potential biomarker for CSF in the future.

Coronary slow flow is taken to be indicative of delayed filling of terminal vessels of the coronary arteries in the absence of coronary stenosis, as detected using coronary angiography. Patients suffering from coronary slow flow typically experience recurrent chest pain, thereby markedly affecting their quality of life. The etiology and pathogenesis of coronary slow flow, which is gradually attracting clinical attention, have yet to be sufficiently established, although it is currently believed that they may be associated with endothelial dysfunction in the coronary arteries, inflammatory response, abnormalities in microvascular reserve function, subclinical atherosclerosis, blood cell and platelet abnormalities, and genetic factors. In this review, we provide a brief overview of recent progress in research on the pathogenesis of coronary slow flow with a view toward elucidating the possible underlying pathogenesis and identify targets and directions for the treatment of this condition.

Cryoballoon ablation (CBA) is recommended for patients with symptomatic drug refractory paroxysmal atrial fibrillation (pAF). However, substantial atrial fibrillation (AF) recurrence is common during follow-up. Searching for a potential biomarker representing both myocardial injury and inflammation to identify patients at high risk of AF recurrence after CBA is very meaningful for postoperative management of AF patients.To evaluate the clinical efficacy of high-mobility group box 1 (HMGB1) protein released from the left atrium to predict AF recurrence in pAF patients after CBA at 1-year follow-up.We included 72 pAF patients who underwent CBA. To determine the expression levels of HMGB1, left atrial blood samples were collected from the patients before CBA and after the procedure through the transseptal sheath. Patients were followed up for AF recurrence for 1 year.A total of 19 patients of the 72 experienced AF recurrence. The level of postoperative HMGB1 (HMGB1post) was higher in the AF recurrence group than in the AF non recurrence group (p = .03). However, no differences were noted in the levels of other biomarkers such as preoperative high-sensitivity C-reactive protein (hs-CRP), postoperativehs-CRP, and preoperative HMGB1 between the two groups. Multiple logistic regression analysis revealed that a higher level of serum HMGB1post was associated with AF recurrence (odds ratio: 5.29 [1.17-23.92], p = .04). Receiver operating characteristic analysis revealed that HMGB1post had a moderate predictive power for AF recurrence (area under the curve: 0.68; sensitivity: 72%; and specificity: 68%). The 1-year AF-free survival was significantly lower in patients with a high HMGB1post level than in those with a low HMGB1post level (hazard ratio: 3.81 [1.49-9.75], p = .005).In pAF patients who under went CBA, the level of HMGB1 after CBA was associated with AF recurrence and demonstrated a moderate predictive power. Thus, we offer a potential biomarker to identify pAF patients at high risk of AF recurrence.

The purpose was to evaluate left ventricular (LV) systolic function in patients with coronary slow flow (CSF), and compared the incremental values of 3-dimensional (3D) speckle-tracking echocardiography (STE). Seventy-three patients with CSF and 60 control subjects were enrolled. CSF was diagnosed during coronary angiography. Two-dimensional (2D) and 3D global strain were measured using STE. Sex, mitral E, 2D GLS, and all 3D strain parameters were independent predictors of CSF. Combination of sex, mitral E, and 3D GTS had the highest area under the curve (AUC) for identifying CSF (AUC, 0.81; P < 0.001). Integrated discrimination index (IDI) improved adding 3D GTS to the combined sex and mitral E model (IDI = 0.12, P = 0.01) or 2D GLS model (IDI = 0.14, P < 0.001). LV systolic function was impaired in CSF patients. 3D GTS had an independent and incremental value for predicting CSF compared with 2D echocardiography.